Dina Schneider
VP, head of Discovery Cartesian
In my current role with Cartesian Therapeutics I am responsible for execution of our company’s R&D Discovery strategy. Namely, I lead a division focused on the discovery and development of novel non-viral cell therapies for autoimmune disease, from inception to IND nomination. In my previous role as the Director of Immuno-Oncology and Cell Therapy at Lentigen Technology, Inc., a Miltenyi Biotec Company, I oversaw the discovery and pre-clinical development of chimeric antigen receptor (CAR) cell therapies for hematologic and solid tumors, and autoimmune disease. Among our successes were the development of Miltenyi’s lead investigational product Zamtocabtagene Autoleucel, and CAR19 employed in the first in the world efficacious and safe CAR T cell therapy for autoimmune disease. During my ten-year tenure with Miltenyi, I authored multiple patents for CAR T cell technology and helped initiate and manage several IIT clinical trials using the CliniMACS Prodigy platform for automated cell manufacturing.
Seminars
This workshop will critically evaluate the translational limitations of in vitro and in vivo models in MG, CIDP, GBS and MMN. While MG may be comparatively easier to model, CIDP and GBS rely on complicated induction systems that do not reliably reflect human immunologic origin, heterogeneity or anatomical distribution. By directly interrogating how current models oversimplify antibody-driven pathology, fail to capture unknown autoantibody subsets (particularly in CIDP/MMN), and may not represent disease compartments such as spinal involvement, developers can recalibrate go/no-go decisions earlier in the pipeline. Attendees will redefine what constitutes meaningful translational evidence, ensuring that preclinical immune modulation signals correlate with functional muscle improvement and clinically relevant biomarkers before advancing assets into heterogeneous patient populations.
Key Questions to be Addressed:
- Analyzing how current in vivo induction methods fail to accurately reflect human disease mechanisms, particularly in CIDP and GBS
- Comparing situations in which developers bypass animal models entirely and evaluating when that strategy is justified
- Embedding clinically relevant biomarkers into preclinical assays to improve forward and reverse translation
- Defining what constitutes a translatable efficacy signal rather than an isolated model-specific response
- Preventing the premature elimination of candidates due to poor model representativeness rather than flawed human biology
